Classification

Higher order taxa

Species

Description and significance

Mycoplasma capricolum belongs to the genus Mycoplasma, which is a genus of bacteria that does not have cell wall or murein. This spherical organism is distinguished from other bacteria by its small size (a characteristic of the genus Mycoplasma) and requirement of cholesterol for growth. However, its DNA structure suggests that Mycoplasma capricolum is derivative of Gram-positive bacteria [8]. Though hard to isolate, this microorganism still can be obtained from lungs and pleural fluid of affected animals in necropsy and is readily cultured in cholesterol and serum-containing medium [9].

Genome structure

Mycoplasma capricolum has a circular genome whose size is 1155.5 kb. Its 25% of GC content is relatively low compared to other organisms. This organism has only one chromosome. Though plasmids are unusual among Mycoplasma species, M. capricolum is found to have a plasmid whose size is around 1.1kb-1.8kb.The extrachromosomal DNA may contribute to antimicrobial resistance since it is found more often in herds that have undergone the use of antimicrobial drugs [7].

Cell structure and metabolism

M. capricolum has no cell wall but only a lipid bilayer membrane, up to 2/3 of unesterified cholesterol is in the outer membrane. It does not have pili or flagella.
This species requires external sources of cholesterol for growth (ie. a natural fatty acid auxotroph), nonetheless, the uptaken fatty acid is not used as substrate for energy production but for phospholipd synthesis instead. The cholesterol is first incorporated into the outer part of membrane then translocated to the inner half.[16] Some experiments also suggest that fatty acid incorporation efficiency is influenced by the concentration of glucose and glycerol, temperature and external pH.[10] Its membrane lipid composition is deduced to be 60% of phosphatidylglycerol and 35% of cardiolipin.[15] M. capricolum can grow on various sterol-containing media, though with different growth rates [14].

Ecology

The natural transmission pathway of M. capricolum is through inhalation of infectious droplets, though infection can be achieved through injecting cell culture experimentally. When inhaled, it is bound by the host cell membrane and its surface-exposing lipoproteins induce strong antigenic reactions. However, its sophisticated antigenic variation makes it hard for the host immune system to produce proper antibodies to suppress the infection. An extracellular polysaccharide structure may have capsule-like function.

Pathology

M capricolum is a causative agent of caprine respiratory diseases, mastitis and severe arthritis. The infection often leads to destructive results in Africa and Asia goat farming industry. Fever is also observed at the end of incubation period. Some subspecies of Mycoplasma capricolum, for example,M. capricolum subsp. mycoides and M. capricolum subsp.capripneumoniae are especially virulent. The morbidity and mortality rate of some subspecies is of 60%-70%. Long-term survival is possible but often accompanied with pleuropneumonia or chronic pleurutis. This bacterium is capable of stimulating macrophages to produce oxygen radicals, TNF-α, IL-6 and nitric oxide. This combination leads the production of peroxynitrite, a very strong oxidant.[4]
For the subspcies M. capricolum subsp.capripneumoniae infection, hepatized lesions and necrosis are observed in the lungs. [5]Nevertheless, M capricolum does not cause systemic reaction.[17] As mentioned before, when M capricolum is inhaled, it is bound by the host cell membrane. Consequently, the inflammatory may be a result of acinar epithelial cells attachment of the bacteria. Nutrient absorption of M capricolum from the host cell membrane is probably the initiation of infection. The toxic oxidant accumulation and the hydrolytic enzymes produced by this species also contribute tissue damage [17]. Tissue fibrosis is recorded.

Application to Biotechnology

The membrane of M. capricolum contains factors that are capable of activating cellular macrophage TNFα, which is a tumor necrosis factor. The macrophage could be induced by other bacterial lipopolysaccharide, but this method is limited in application due to the toxicity of bacterial lipopolysaccharide. The relatively stable membrane of M. capricolumis found to be an especially potent and non-lipopolysaccharide activator of macrophage, thus it may have therapeutic value in treating cancer [11].

Current Research

Various studies of Mycoplasma capricolum are under process. Those projects include antimicrobials effect[6], which is determined by flow cytometry techniques. One of these evaluating experiments is done in Turkey to evaluate the efficacy of the drug, danofloxacin (Advocin A180) on goats. The result indicates that this treatment may be able to prevent the spread of Mycoplasma capricolum. [12]
Mycoplasma capricolum is also used in an experiment on the incorporation of non-natural amino acids into proteins(ie. amber suppression tRNA experiment). Due to the low incorporation efficiency, the application of amber suppression is limited.M. capricolum is proven to be able to contain tRNA with high specificity. [13]